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. Author manuscript; available in PMC: 2022 Dec 1.
Published in final edited form as: Hypertension. 2022 Mar 17;79(6):1190–1202. doi: 10.1161/HYPERTENSIONAHA.121.17245

Figure 5.

Figure 5.

Responses of key components of the renin-angiotensin-system in urine and the kidney of EP1fl/flAqp2Cre− and EP1fl/flAqp2Cre+ mice during normal-Na+ (NS) and low-Na+ (LS) intake. (A) The urine samples were assayed for total renin/prorenin, renin activity, and angiotensin II (Ang II). N=10 per group. Data are mean ± SEM. *p<0.05, **p<0.01 vs. NS; #p<0.05, ##p<0.01, ###p<0.001 vs. EP1fl/flAqp2Cre− (ANOVA with the Bonferroni test). (B) Representative immunoblotting and densitometric analysis of (Pro)renin receptor (PRR) and prorenin expression in the renal cortex and medulla with β-actin as an internal control. Prorenin-probed membranes were probed with anti-β-actin antibody. N = 3–4 per group for statistical analysis. Data are mean ± SEM. *p<0.05, **p<0.01, ***p<0.001 vs. NS; #p<0.05, ###p<0.001 vs. EP1fl/flAqp2Cre− (ANOVA with the Bonferroni test). (C) RT-qPCR analysis of PRR and renin mRNA in the renal cortex and medulla with GAPDH as an internal control. N = 5 per group. Data are mean ± SEM. **p<0.01 vs. EP1fl/flAqp2Cre−+NS; ##p<0.01 vs. EP1fl/flAqp2Cre++NS, $ $ $p<0.001 vs. EP1fl/flAqp2Cre−+LS (ANOVA with the Bonferroni test).